Koebner phenomenon

Source = Wikipedia

Koebner phenomenon = skin lesions appearing on lines of trauma. It may result from either linear exposure or linear irritation.

Linear exposure:

• Molluscum contagiosum (auto-inoculation)
• Warts (auto-inoculation)
• Toxicodendron dermatitis (e.g. poison ivy... linear from brushing against plant).

Linear irritation, e.g. scratching or surgical wound:

• Psoriasis*
• Eczema*
• Lichen planus*
• Vitiligo*
• Lichen nitidus
• Lichen sclerosus
• Pityriasis rubra pilaris
• Keratosis follicularis
• Elastosis perforans serpiginosa.

*4 most common causes of Koebner phenomenon = PELV

The Koebner phenomenon was named after a rather eccentric, renowned German dermatologist, Heinrich Koebner (1838–1904). Koebner is best known for his work in mycology. Here is one story to illustrate his intense nature: in a medical meeting he proudly exhibited on his arms and chest three different fungus infections, which he self-inoculated in order to prove the infectiousness of the organisms he was studying.

Psoriasis pathology

Source: Robbins 840

Affects 1-3% of people.

Psoriasis is an immunologic disease with contributions from genetic susceptibility and genetic factors. It is not known if the inciting antigens are self or environmental.

Sensitised populations of T cells enter the skin, including dermal CD4+ TH1 cells and CD8+ T cells that accumulate in the epidermis.

T cells homing to the skin secrete cytokines and growth factors that induce keratinocyte hyper-proliferation, resulting in the characteristic lesions.

Psoriatic lesions can be induced in susceptible individuals by local trauma, a process known as the Koebner phenomenon. The trauma may induce a local inflammatory response that promotes lesion development.

Morphology

• Marked epidermal thickening (acoanthosis).
• Regular donward elongation of the rete ridges. This downward growth has been likened to test-tubes in a rack.
• Increased epidermal cell turnover and lack of maturation results in loss of the stratum granulosum with extensive overlying parakeratotic scale.
• There is thinning of the epidermal cell layer overlying the tips of dermal papillae (suprapapillary plates).
• Blood vessels within the papillae are dilated and tortuous. These vessels bleed rapidly when the scale is removed, giving rise to multiple punctate bleeding points (Auspitz sign).
• Neutrophils form small aggregates within both the spongiotic superficial epidermis (pustules of Kogoj) and the parakeratotic stratum corneum (Munro microabscesses).
• Similar changes can be seen in superficial fungal infections, and it is important to exclude this possibility with special stains in new diagnoses of psoriasis.

Psoriasis most frequently affects the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal cleft, glans penis.

The most typical lesion is a well-demarcated, pink plaque covered by loosely adherent silver-white scale.

Nail changes occur in 30% and consist of yellow-bown discoloration, with pitting, thicking and onycholysis (crumbling and separation of the nail bed from the underlying bed).

There are a variety of clinical subtypes.

Management of psoriasis

Source: Wikipedia

1. Cognitive behaviour therapy

2. Topical Rx

Bath solutions and moisturizers, mineral oil, and petroleum jelly may help soothe affected skin and reduce the dryness which accompanies the build-up of skin on psoriatic plaques. Ointments and creams containing coal tar, dithranol (anthralin), corticosteroids like desoximetasone (Topicort), fluocinonide, vitamin D3 analogues (for example, calcipotriol), and retinoids are routinely used. Argan oil has also been used with some promising results. The mechanism of action of each is probably different but they all help to normalise skin cell production and reduce inflammation. Activated vitamin D and its analogues are highly effective inhibitors of skin cell proliferation.

The disadvantages of topical agents are variably that they can often irritate normal skin, can be time consuming and awkward to apply, cannot be used for long periods, can stain clothing or have a strong odour. As a result, it is sometimes difficult for people to maintain the regular application of these medications. Abrupt withdrawal of some topical agents, particularly corticosteroids, can cause an aggressive recurrence of the condition. This is known as a rebound of the condition.

Some topical agents are used in conjunction with other therapies, especially phototherapy.

3. Phototherapy

Daily, short, non-burning exposure to sunlight helped to clear or improve psoriasis in some patients. Niels Finsen was the first physician to investigate the therapeutic effects of sunlight scientifically.

Ultraviolet wavelengths are subdivided into UVA (380–315 nm) UVB (315–280 nm), and UVC...

4. Photochemotherapy

Psoralen and ultraviolet A phototherapy (PUVA) combines the oral or topical administration of psoralen with exposure to ultraviolet A (UVA) light. Precisely how PUVA works is not known. The mechanism of action probably involves activation of psoralen by UVA light which inhibits the abnormally rapid production of the cells in psoriatic skin. There are multiple mechanisms of action associated with PUVA, including effects on the skin immune system.

PUVA is associated with nausea, headache, fatigue, burning, and itching. Long-term treatment is associated with squamous cell carcinoma (not with melanoma).

5. Systemic treatment

Psoriasis that is resistant to topical treatment and phototherapy is treated with systemic treatment. Patients undergoing systemic treatment are required to have regular blood and liver function tests because of the toxicity of the medication. Pregnancy must be avoided for the majority of these treatments. Most people experience a recurrence of psoriasis after systemic treatment is discontinued.

The three main traditional systemic treatments are methotrexate, cyclosporine and retinoids. Methotrexate and cyclosporine are immunosuppressant drugs; retinoids are synthetic forms of vitamin A.

Other additional drugs, not specifically licensed for psoriasis, have been found to be effective. These include the antimetabolites tioguanine, mercaptopurine and fluorouracil, the cytotoxic agents hydroxyurea and paclitaxel, alkylating agents chlorambucil and cyclophosphamide, some DMARDs like sulfasalazine, colchicine, dapsone, the immunosuppressants mycophenolate mofetil, azathioprine and oral tacrolimus. These have all been used effectively to treat psoriasis when other treatments have failed.

Although not licensed in many other countries, fumaric acid esters have also been used to treat severe psoriasis in Germany for over 20 years.

There is also some evidence for beneficial effect on psoriasis of insulin-sensitizing drugs (thiazolidinediones like pioglitazone and rosiglitazone, and a more modest effect is described for metformin), somatostatin, bromocriptine, and some lipid-lowering drugs from the group of statines (like simvastatin), and omega-3 fatty acid supplements. For all those drugs it is hypothesised that their antipsoriatic activity comes from their immunomodulatory properties.

There are also case reports and small trials describing beneficial effects of yohimbine (effect is thought to be secondary to its insulin-lowering and growth hormone lowering properties), ketotifen (effect is thought to be secondary to its ability to dampen release of inflammatory mediators) and albuterol (beta-adrenergic agonist).

Antihistamine drugs generally do not help to improve psoriasis lesions, but they may be of use to reduce itching and also are helpful in cases where psoriasis coexists with skin allergy, for example chronic urticaria. Some antihistamines have sedative properties, thus might aid to improve sleep and reduce anxiety in psoriasis patients.

Antidepressant medications may help to reduce comorbid depression, anxiety, social isolation, improve sleep and in some cases reduce itching (primarily due to antihistamine effects of tricyclic antidepressants and some SSRIs). Naltrexone, an opioid antagonist, and pregabalin or gabapentin, benzodiazepine anxiolytics are also of use in severe itching.

NSAIDs generally do not help to improve psoriatic arthritis itself, but they might provide rapid symptomatic relief from pain and swelling.

Biologics are manufactured proteins that interrupt the immune process involved in psoriasis. Unlike generalised immunosuppressant therapies such as methotrexate, biologics focus on specific aspects of the immune function leading to psoriasis. These drugs (interleukin antagonists) are relatively new, and their long-term impact on immune function is unknown, but they have proven effective in treating psoriasis and psoriatic arthritis. They include Amevive, Enbrel, Humira, Remicade and Raptiva. Raptiva was withdrawn by its maker from the US market in April, 2009. Biologics are usually given by self-injection or in a doctor's office. They are very expensive and only suitable for very few patients with severe psoriasis. Ustekinumab (IL-12 and IL-23 blocker) shows hopeful results for psoriasis therapy.

Noting that botulinum toxin has been shown to have an effect on inhibiting neurogenic inflammation, and evidence suggesting the role of neurogenic inflammation in the pathogenesis of psoriasis, the University of Minnesota has begun a clinical trial to follow up on the observation that patients treated with botulinum toxin for dystonia had dramatic improvement in psoriasis.

Classification of psoriasis

Source: Wikipedia

In contrast to eczema, psoriasis is more likely to be found on the outer side of the joint.
Some patients have no dermatological symptoms.
Local psoriatic changes can be triggered by an injury to the skin - Koebner phenomenon.

Psoriasis is classified into nonpustular and pustular types:

Non-pustular

• Psoriasis vulgaris: a.k.a. plaque psoriasis. The most common type (80%-90% of patients). Raised areas of inflamed skin covered with silvery white scaly skin.
• Psoriatic erythroderma: Inflammation and exfoliation of skin over most of the body. May be accompanied by severe itching, swelling and pain. It is often the result of an exacerbation of unstable plaque psoriasis, particularly following the abrupt withdrawal of systemic Rx. Can be fatal, as the extreme inflammation and exfoliation disrupt the body's ability to regulate temperature and for the skin to perform barrier functions.

Pustular

Pustular psoriasis appears as raised bumps filled with non-infectious pus (pustules). The skin under and surrounding the pustules is red and tender. Can be localised, commonly to the hands and feet (palmoplantar pustulosis), or generalised with widespread patches occurring randomly on any part of the body. This classification includes:

• Generalised pustular psoriasis (of von Zumbusch)
• Pustulosis palmaris et plantaris
• Annular pustular psoriasis
• Acrodermatitis continua
• Impetigo herpetiformis (a form of severe pustular psoriasis occurring in pregnancy).

Other

• Drug-induced.
• Inverse psoriasis, a.k.a. flexural psoriasis. Occurs in skin folds, particularly around the genitals (between the thigh and groin), armits under an overweight stomach (pannus) under the breasts (inframammary fold). Aggravated by friction and sweat, and is vulnerable to fungal infections.
• Napkin psoriasis.
• Seborrhoeic-like psoriasis.
• Guttate psoriasis: Numerous small, scaly, red/pink, teardrop-shaped lesions over large areas of the body, primarily the trunk (also limbs and scalp). Often preceded by a streptococcal infection, typically streptococcal pharyngitis.
• Nail psoriasis: Discolouring, pitting, lines going across the nails, thickening of skin under nail, loosening and crumbling of the nail (onycholysis).
• Psoriatic arthritis: Joint and connective tissue inflammation. Can affect any joint but most common in the joints of fingers and toes. Can result in sausage-shaped swilling of fingers/toes (dactylitis). Can also affect the hips, knees and spine (spondylitis). 10%-15% of people with psoriasis have psoriatic arthritis.